Dementia Flashcards
(41 cards)
Dementia
an acquired syndrome of decline in memory and other cognitive functions sufficient to affect daily life in an alert person, usually behavioral disturbances too
Diagnosis of dementia
DSM-V-TR, spouse, rating scales, autopsy, brain atrophy and neuronal loss (dec acteylcholine)
Risk factors of dementia
age, fam hx, hx of head trauma
Alzheimer’s disease
60-70% of all dementias, presence of B-amyloid and tau proteins, slow, progressive decline in cog ability, initial impairment w/ short term memory, difficulty learning new info, aphasia, impaired visuospacial fct
Lewy Body Dementia
Lewy body plaques, limbic and neocortical areas outside the substantia nigra, presents w/ fluctuations in alertness/attentian and confused states, visual hallucination are common, parkinsonia, orthostatic hypoTN, syncope
Vascular dementia
abrupt onset with stepwise, causal decline in cog function, based on vascular insults, language and memory retrieval difficulties, symptoms largely reliant on location of injury
parkinson’s dementia
pts w/ parkinson’s have 6x chance of dementia diagnosis, motor disturbances accompanies and often precedes symptoms, gait dysfunction, visual disturbances, frequent falls
What should you avoid when possible
antihistamine, oxybutnin, tolterodine, cyclobenzaprine, TCAs
AD treatment of cog sx
acetylcholinesterase inhibitors, NMDA antagonist
AD treatment of BPSD
non-pharm therapy, antipsychotics, antidepressants, antionvulsants/ mood stabilizers, benzos
Non-pharm treatment
exercise body/brain, mediterranean diet, music, orientation reinforcement, communication, attention to safety
Basic principles of care for AD
Keep requests and demands simple, avoid confrontation, remain calm, firm, supportive, frequent reminders, explanations, orientation cues, adjust to expectations, patience!
AChEI aimed to
increase acetylcholine, correct the cholinergic deficiency hypothesis of amnesia
Nucleus basalis of meynert
located in basal forebrain, principle site of cholinergic cell bodies for axons that project to the hippocampus, amygdala and throughout the neocortex, it is the degeneration of these cells that leads ot AD
MOA of AChEI
inhibit acetylcholinesterase, inhibit degradation of acetylcholine and thus increase acetylcholine concentrations in nerve synapses, doesn’t affect underlying neurodegenerative process
Efficacy of AChEIs
most effective when started early, used for mild to moderate, and moderate to severe AD; may see benefit for 1-3 years
ADRs of AChEIs
nausea, vomiting, diarrhea, wt loss, can exacerbate GI bleed
AChEIs
Donepezil (Aricept), Rivastigmine (Exelon), Galantamine (Razadyne), combo Donepezil/Memantine (Namzaric)
Donepezil (Aricept)
better tolerated and more convenient dosing, indicated for mild to severe AD, CNS selective, reversible inhibitor of AChE
Dosing of Donepezil (Aricept)
5 mg qHS for 4-6 weeks, then increase to 10 mg qHS
Rivastigmine (Exelon)
less tolerable compared to donepezil, less DI, CNS selective, pseudo-irreversible for AChE and BuChE, mild to severe AD and Parkinson’s dementia, hard on GI
Rivastigmine (Exelon) patch
less GI SE, better for compliance, 4.6mg/24 hours (4 weeks, can titrate up) and 9.5mg/24 hours
Galantamine (Razadyne)
reversible, competitive AChEI, more DIs, 3A4 & 2D6 metabolism, should not be used in severe renal and hepatic impairment, mild to moderate disease
Memantine (Namenda) effects
block Ca entry when extracellular glutamate is low, allows intracellular Ca levels to return to normal, when glutamate is increased in response to an action potential, glutamate displaces memantine, causing brief Ca entry
